Regulatory T cells promote a protective Th17-associated immune response to intestinal bacterial infection with C. rodentium.
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Authors
Wang, ZFriedrich, C
Hagemann, S C
Korte, W H
Goharani, N
Cording, S
Eberl, G
Sparwasser, Tim
Lochner, M
Issue Date
2014-11
Metadata
Show full item recordAbstract
Intestinal infection with the mouse pathogen Citrobacter rodentium induces a strong local Th17 response in the colon. Although this inflammatory immune response helps to clear the pathogen, it also induces inflammation-associated pathology in the gut and thus, has to be tightly controlled. In this project, we therefore studied the impact of Foxp3(+) regulatory T cells (Treg) on the infectious and inflammatory processes elicited by the bacterial pathogen C. rodentium. Surprisingly, we found that depletion of Treg by diphtheria toxin in the Foxp3(DTR) (DEREG) mouse model resulted in impaired bacterial clearance in the colon, exacerbated body weight loss, and increased systemic dissemination of bacteria. Consistent with the enhanced susceptibility to infection, we found that the colonic Th17-associated T-cell response was impaired in Treg-depleted mice, suggesting that the presence of Treg is crucial for the establishment of a functional Th17 response after the infection in the gut. As a consequence of the impaired Th17 response, we also observed less inflammation-associated pathology in the colons of Treg-depleted mice. Interestingly, anti-interleukin (IL)-2 treatment of infected Treg-depleted mice restored Th17 induction, indicating that Treg support the induction of a protective Th17 response during intestinal bacterial infection by consumption of local IL-2.Citation
Regulatory T cells promote a protective Th17-associated immune response to intestinal bacterial infection with C. rodentium. 2014, 7 (6):1290-301 Mucosal ImmunolAffiliation
Institute of Infection Immunology, TWINCORE, Centre for Experimental and Clinical Infection Research,Feodor-Lyner-Str. 7, 30625 Hannover, Germany.Journal
Mucosal immunologyPubMed ID
24646939Type
ArticleLanguage
enISSN
1935-3456ae974a485f413a2113503eed53cd6c53
10.1038/mi.2014.17
Scopus Count
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